Meet Mark

Let me introduce myself. My name is Mark Sisson. I’m 63 years young. I live and work in Malibu, California. In a past life I was a professional marathoner and triathlete. Now my life goal is to help 100 million people get healthy. I started this blog in 2006 to empower people to take full responsibility for their own health and enjoyment of life by investigating, discussing, and critically rethinking everything we’ve assumed to be true about health and wellness...

Could Gut Bacteria Be to Blame for Your Stubborn Belly Fat?

We know how important gut health is for overall health. We understand that it improves digestion, that our pursuit of extreme sterility has compromised our immune systems, and that the gut biome is etiologically involved in the pathogenesis of various health and disease states. We’re even familiar with the more esoteric functions of gut bacteria, like converting antinutrients into biovailable nutrients, synthesizing sex hormones and neurotransmitters, and mitigating the allergenicity of gluten. But what about gaining and losing body fat, the real reason most people get interested in diet in the first place—are the bacteria in your gut responsible for the fat on it?

Maybe.

The animal literature shows that direct manipulation of the gut biome can affect bodyweight and resistance to obesity. In one paper, transplanting gut bacteria from obese mice into lean mice led to a 60% increase in body fat and a rapid, 14-day descent into insulin resistance following the gut flora alteration. Another found that mice seeded with bacteria from lean mice even appear resistant to developing obesity when consuming fecal matter (a basic, if disgusting form of fecal transplant) from obese mice. At least in mice, “obese gut bacteria” and “lean gut bacteria” are well-established and appear to be causally-related to body weight.

In humans, the evidence is more mixed. Some studies find a higher proportion of Firmicute bacteria and fewer bacteria from the Bacteroidete family in the obese and overweight, while others find the opposite. The only concrete conclusion from a 2012 meta-analysis was that obesity in humans tends to track with an increase in members of the Firmicutes phylum. As for direct interventions, changes to the gut bacteria certainly accompany weight gain, but it’s unclear whether the relationship is coincidental or causal—and if causal, in which direction causality flows. Does obesity change the composition of the gut bacteria? If so, targeting the gut bacteria with diet, probiotics, prebiotics, and other therapies may not have the intended effect.

Indeed, a recent review suggested “that in humans the changes in gut microbiota are an association with rather than the cause of obesity.”

Rather than take their word for it, Let’s examine whether anything mediated by gut bacteria also changes body weight.

Antibiotics

Antibiotics are the first place to look, because alteration of the gut bacteria isn’t a side effect of antibiotics. It’s a feature. The broad-spectrum antibiotics do the most collateral damage, killing good and bad bacteria alike. And there’s good evidence that antibiotics play a role in the development of obesity. For one, farmers have been giving low doses of antibiotics to their livestock to increase weight gain for decades; if it didn’t work, they wouldn’t spend the money on the drugs. In children, antibiotics increase the risk of obesity later in life in a dose-response manner. The more doses they receive, the more obese they get. The earlier they take them, the worse, with “antibiotic exposure before 6 months of age, or repeatedly during infancy, [being] associated with increased body mass in healthy children.” The effect may be strongest in boys.

Fecal Transplant

Although the animal literature confirms that fecal transplantation from an obese rodent to a lean rodent can make the recipient gain weight (and vice versa), only one such example—a case study— exists in humans. A woman with a digestive disorder got a fecal transplant from her overweight daughter. It cured the disorder but the woman soon became obese, too.

Another human study gave 18 obese Dutch men with metabolic syndrome fecal transplants from lean donors. They did not lose weight, but they did experience improved insulin sensitivity and triglyceride numbers. These improvements reverted after about 12 weeks, probably because they maintained the diet that got them obese in the first place.

Probiotics

Earlier this year, an RCT found that giving overweight subjects two daily doses of L. curvatus HY7601 and L. plantarum KY1032 reduced body fat and waist circumference without affecting food intake or increasing exercise. It doesn’t look like body weight decreased, but that’s good news; it means fat was lost and lean mass retained or even increased. As a nice benefit, the probiotic group also experienced lower levels of oxidized LDL and saw their LDL particle size increase. L. plantarum is one of the strains I include in Primal Probiotics (formerly known as Primal Flora).

Some researchers propose limiting probiotics in obese people to avoid weight gain via increased bacterial biomass, which most estimates say can weigh between 2 to 6 pounds. That’s like worrying about weight gain from increased muscle hypertrophy and bone mineral density. It’s also a valid confounder for weight loss in prebiotic and probiotic studies. If a person nurtures their gut and gains four pounds of bacterial biomass, that will show up on the scale and could, unless you’re measuring waist circumference or body fat percentage, throw off the measurement of effect.

Lipopolysaccharide (LPS)

LPS is a bacterial endotoxin produced when gram-negative bacteria die off in the gut. It’s implicated in leaky gut and, at least in animal studies, can exacerbate or even initiate obesity by increasing systemic inflammation and insulin resistance.

How can your gut biome affect the amount of LPS you produce—or admit to systemic circulation?

First, beneficial gut bacteria take up space along the gut wall, effectively forming a barrier to entry by pathogens. A healthier and more robust gut biome means there’s less room for LPS to slip through the tight junctions into wider circulation.

Third, providing enough fermentable fiber for your gut bacteria to eat means they’re less likely to consume the mucin protecting the gut lining from invasion. If you starve your gut bacteria, they will begin eating the mucosal barrier and open you up to LPS toxicity.

A common refrain you often hear is that “high-fat diets induce LPS toxicity.” And yeah, looking at most of the available literature, that appears to be true. Lipopolysaccharide rides along and absorbs better with fat. It’s right there in the prefix: “lipo.”

But a recent paper found that when you give mice whole foods-based diets rather than refined diets, the fat content has no bearing on LPS toxicity. If anything, increased dietary fat through whole foods increasedmucin production and reduced LPS toxicity.

Diet

Several studies have wondered if changing the diet to include more fermentable fiber and shape the gut biome can reduce obesity, but there’s a problem with this approach: changing the diet changes the diet. There’s really no way to know if the change to gut bacteria is responsible for the change in bodyweight or if the diet is changing the bodyweight which changes the gut bacteria. You can’t easily disentangle the two.

In a recent paper, hospitalized obese kids were placed on a diet rich in fermentable fiber. Significant reductions in body weight were accompanied by concomitant alterations to the gut bacteria. Transplanting gut microbes from one pre-intervention obese kid into germ-free mice increased adiposity and inflammation compared to transplanted microbes from the same kid post-intervention. Looks promising, but we need to see what happens when those pre- and post-intervention microbes are transplanted into another human. Another study by the same team placed obese adult subjects on similar diets, finding the same results.

In both cases, the new diets changed more than just the fermentable fiber content. They also incorporated “TCM food plants that are rich in dietary fiber, including adlay (Coix lachrymal-jobi L.), oat, buckwheat, white bean, yellow corn, red bean, soybean, yam, big jujube, peanut, lotus seed, and wolfberry,” as well as an extract of bitter melon, a medicinal food with suspected anti-diabetic effects. These are foods and supplements with bioactive compounds that likely affect obesity and metabolism apart from the fiber content. They may very well reduce obesity, but we cannot confirm that bacterial alterations are responsible.

Prebiotics

Consumption of fiber that nourish our gut bugs—prebiotic, fermentable fibers and starches—appears to have anti-obesity effects.

One study found that oligosaccharides, another class of prebiotics, increased satiety hormones and led to weight loss in overweight people. The low-prebiotic control group gained weight and had no improvement in hunger. However, calorie intake wasn’t controlled, so the prebiotic group ate fewer calories (because they weren’t as hungry) and thus lost weight. Skeptics would say, “See, it was calories all along!” I say, “Yeah, but the prebiotics made the calorie reduction sustainable!”

Although the direct clinical evidence is lacking, it’s reasonable to assume that improving insulin sensitivity, increasing production of satiety hormones, reducing excess cortisol, and potentially increasing energy expenditure via short chain fatty acid production could help a person lose weight.

That said, a recent study raises the possibility of fiber behaving badly in a certain segment of the population. In a group of mice, scientists removed the genes coding for toll-like receptor 5 (TLR5), which keeps pathogenic microbes from entering circulation, is a major component of the innate immune system protecting against infections, and prevents bacterial overgrowth. Mice without TLR5 are prone to developing inflammatory bowel diseases, fatty liver, and metabolic syndrome. In this latest study, the TLR5-knockout mice developed the worst cases of metabolic syndrome in response to dietary fiber.

And those mice who got the worst cases of metabolic syndrome also produced the most short-chain fatty acids (SCFAs). SCFAs are the product of bacterial fermentation of dietary fiber. There are three major kinds: butyrate, which is primarily used by colonic cells and has a consistent link to improved metabolic health; propionate, a substrate for gluconeogenesis (glucose synthesis) in the liver; and acetate, 70% of which ends up in the liver as substrate for long-chain fatty acid synthesis. The lack of TLR5 led to unchecked bacterial overgrowth, and the teeming masses of bacteria were overproducing short-chain fatty acids which were stimulating the creation of new fat in the liver. Based on the metabolic fate of various SCFAs, excess acetate was the likely culprit. Many experts believe fatty liver sets a person up for type 2 diabetes and obesity.

These were mice, though. While TLR5-knockout mice get fat on fibrous diets, humans without TLR5 are actually less likely to become obese and more likely to get type 2 diabetes. Obesity is in many respects a defense mechanism for bodies overburdened with available energy; it’s safer to store excess nutrients in body fat than to let free fatty acids and glucose circulate indefinitely. TLR5 issues are certainly bad for people, but I don’t think many people have to worry about getting fat from fermentable fiber.

My gut sense is that the gut biome is a factor in weight loss, but probably not the biggest. But around the margins? For people who just need to tweak something for those stubborn few pounds? Normalizing testosterone levels, tamping down elevated cortisol, boosting satiety hormones, improving insulin sensitivity, increasing beneficial gut bacteria, and reducing lipopolysaccharide toxicity can all, in a roundabout way, help you lose weight and improve your metabolic health and resistance to obesity.

Can you give some good, practical examples of prebiotic foods? I am taking in RS in the form of potato starch and it seems to be beneficial (or at least not harmful) but I know there are other options as well. I just don’t think I can eat that much raw garlic (or the people around me would appreciate it).

Any suggestions on ways to get other prebiotics in or supplements (inulin?)

I take a half a green banana every other day or so because they are lower in carbs and higher in good starch than a ripe one. About an hour later I pop an excellent probiotic and usually eat some sauerkraut…super effective for me and my clients I coach

I think it’s quite possible that gut bacteria can make it difficult to lose weight, but gaining weight in the first place is all about what we eat. There simply isn’t any way to become fat other than by putting food in our mouths. Thyroid problems, medications, gut bacteria, etc. can make it necessary to adjust portion amounts, but the bottom line is still going to be what and how much we eat. For me, it was wheat products that were the main culprit. When I lost the wheat I also lost the weight and have kept it off.

Maybe “weight” is the wrong word to use since I rarely ever weighed myself and still don’t. (What good is weight loss if you still look like a marshmallow on a stick and feel worse than ever?) My method was to stand naked in front of a full-length mirror once a week and be brutally honest in my assessment. I dropped two clothing sizes after I began avoiding wheat, but it was more a case of regaining a waistline, a flat tummy, better muscle definition, and curves that weren’t nearly so curvy.

I had that same experience, Shary. When I lost the wheat, and also added sugar, I lost weight and kept it off. I wasn’t really “over-weight” to begin with according to BMI numbers, but I could see a pop gut starting, and had small love handles that I found unsightly.

Thanks for a reasoned analysis in this area. I am increasing my resistant starch intake, but I haven’t found many benefits yet. I have noticed I think I sleep better, however, I’m also having a harder (not easier) time going to the bathroom. I’m going to try to increase the RS content of my diet for another 1-2 months to see if there’s any improvement.

Here’s another primer about RS, and this includes a list of RS-containing foods:

My personal opinion about the free the animal website is that the author is too invested in the theory that RS is good. I prefer someone who approaches science with a cautious mind, and the author of that (free the animal) website does not in my opinion.

That’s why I’m grateful for your piece above, which I find to be cautious.

On the one hand, I could see where RS could be beneficial; on the other hand, why can’t we just eat vegetables without being concerned about their RS content? Why do I have to eat raw potatoes or Bob’s Red Mill potato starch or cold rice or green bananas/plaintains? I live in New England, and I can’t see if I were alive 300+ years ago that there would be a lot of RS foods around. (Though I’m from European ancestry.) If that’s the case, why do we now suddenly need RS?

A word of caution to anyone considering RS supplementation. I jumped on that bandwagon when it first rode into the paleosphere a couple of years ago. I increased dosage slowly, used all the various methods recommended, and did a lot of trial and error. I experienced long, vivid dreams and a noticeable change in quantity and composition of bowel movements. Other than that, I saw no particular benefits.

Then, something went horribly awry. At first, I attributed my bad side effects to adaptation or die-off, but I persisted. Eventually, I had to stop the RS supplementation altogether. The long and short of it is that I ended up with SIBO.

I had had over four years of fantastic digestive health, endless energy, increased immunity, and a host of other benefits from the paleo diet prior to my RS experiment. I had no digestive problems of any kind prior to the RS.

Quitting the RS supplementation was not enough to cure me. I had serious acid reflux, heartburn, indigestion, many new food intolerances, and a host of bizarre emotional, psychological, and physiological side effects.

Eventually, I went on the anti-bacterial protocols and restricted diet recommended by Dr. Allison Siebecker, and managed to overcome the SIBO. I am still cautious with many high-fiber and SCD-illegal foods, but have managed to mostly make my way back to the health, vitality, and freedom I enjoyed on the paleo diet prior to my RS supplementation.

Good point Eric B, I tell anyone that takes NSAIDS to make sure to rebuild their gut because it destroys mine.

And I would like to know how to find this “Another prebiotic, galacto-oligosaccharides (GOS), can lower levels of the stress hormone cortisol.”
so I can lower that …… apparently the stress reduction isn’t working for me…..

I guess I should specify that I’d like to know if I can “eat this” in the form of food, I do potato salad for potato starch but where would this come from, other than a powder from Amazon or someplace in the UK?

If it doesn’t work for you move on. These are research results but as in any diet, if it’still not working for you it’s not working. After 67 years I found what works for ME by taking a little from here and a little from there. I was daring.
I have maintained my weight for 3 years now without starving or exercising to total body breakdown.
In the past I tried every possible diet that was vogue. There is no gospel truth.
Paleo has, by far, been the most effective for me, yet I have modified it to suit my problems, my wants and my needs. I was never obese but always yoyo’d until I customized my own grazing pattern.
My friends talk about their medications, their doctor visits, and yes, sorry to say, their bowel problems. Since modifying my diet to suit myself I don’the have anything to contribute other than
listening. They see me but don’the want to know because they stick to what they learned ages ago. They ask but they don’the do and really don’the want to change. So?….Do what feels right…keep researching and tweaking…this site is full of information, use it but remember, it’s not gospel, just one of the smarter places to be. Good luck to you.
(If this shows up with a lot of nonsense stuff it’s my tablet correct type.)

I completely agree, the thing with these poor lab mice (who spend their short lives in severe intestinal distress, just so humans know not to eat fries with everything) is that they’re a homogenous population, whereas we’re free-range, with our own past histories of antibiotic use, dieting, disease, etc., not to mention varying genetic inheritance.

I worry when I see people eating potato starch or kefir *every* day just because they read on some blog it was the wonderfood – one thing we DO know is that in the past, diets varied widely over the seasons of the year, because you got what was local or could be preserved, and not a daily avocado for example, just because we can now ship them in every day of the year.

It’s my working theory that our bodies evolved the ability to OVER-extract nutrients from food, since they might not be getting that type again for maybe 11 more months, and that this is why regular consumption of any one thing can create low-level intolerance after a while – food isn’t neutral, our bodies have their own reaction (probably like a reversed hockey-stick) to the nutrients whereby regaulr intake of a thing that’s good in short bursts becomes hazardous over a longer period.

Yes, I know I’m not a scientist, but it fits with the availability patterns of our ancestors, and also the way everyone from vegans to hardcore 1972 Atkins dieters report an enormous feeling of wellbeing at the start of their diet (which almost certainly has different nutrients to their former way of eating), followed by a plateau, then often a decline into chronic health issues.

The Primal Blueprint as I understand it is reasonably free of that risk since it emphasises fresh and seasonal food and variations, and that’s why I like it, but I personally am dubious about any daily wonderfood, it just “ain’t natural”!

When I wrote this yesterday, I forgot to add that it’s my working theory that the reason prolonged daily intake of identical foodstuffs is damaging, is because it favours one type of bacteria over the others, causing a long-term imbalance, whereas a varied diet favours different types around the cycle of the year (originally, and now if we aim to eat in-season local food).

I currently suspect that it may be the various byproducts and other metabolic effects of the gut’s biome that really squeeze the most out of the food, to an extent which, if intake is monotonously prolonged, becomes damaging in multiple ways.

You see something similar in dogs and cats who are fed a mono-diet of one variety of processed ready-made petfood, and experience gastro-intestinal upsets if that type is changed (it’s widespread advice to changeover gradually, mixing old and new in different ratios) – I believe this is because gut bacteria etc that are needed to handle different substances found a new formula have been seriously depleted by a mono-diet of one set of nutrients.

That’s my current theory on why bad reactions to what have become never-ending daily staples, like milk, high-gluten wheat, and fruit juices, are now becoming so prevalent, but I’m no scientist, so just shooting this out for other people’s consideration.

Hey mark. I was wondering if there is any research on the interplay between dietary fiber, dietary fat and microbiome composition. For instance if you eat a certain cluster of fibers as a salad, topped with vinegar, how might that differ from eating the same cluster of fibers but coated in butter? Or tallow? Or with nothing at all. I guess what i’m asking is wether dietary fats influence microbiome composition independently of fiber(type, quantity, etc) does increasing butyric acid content of the diet select for a group of gut bugs that tolerate and produce butyric acid?(or other important scfa’s) Are modern animal based foods relatively deplete in important scfa’s in light of the abiotic nature of their lifestyles?

A little besides the point, but I’ve been wondering–what does it mean when links are crossed out? In old posts, some times they aren’t available anymore. But what about in new posts, like this one? Link works…is it not actually a good study?

Great info, but I’m having trouble applying it. It sounds like a lot of the probiotics that scientists are using for research aren’t commercially available- any idea where I can get L. curvatus, L. plantarum, or L. reuteri?

Thanks of the article. For the last month I’ve started to have some probiotics in the morning, in form of miso soup (from barley) . I find it helpful as a way to clean my gut. Probably doesn’t burn much fat , but it helps to remove that bloated sensation so my belly looks better inside and outside.